The hypothesis was tested whether the post-ischemic excitation of neurons, leading to their demise, can be related to a primary effect of ischemia on inhibitory interneurons, particularly on the intrinsic system of GABAergic basket cells in the hippocampus. Their damage would then allow an unrestrained release of glutamate which could ultimately lead to a delayed neuronal death of the post-synaptic neurons, such as it occurs in the CA1 sector of the hippocampus. To test this hypothesis we studied immunohistochemically the presence of the GABAergic innervation in CA1 sector up to 14 days after a 5 minute bilateral occlusion of carotid arteries in gerbil. Assaying immunohistochemically the presence of GABA-synthesizing enzyme glutamate decarboxylase (GAD) our observations revealed that local GABAergic neurons are spared from acute and delayed ischemic effect and that the pattern of GABAergic innervation of the CA1 neurons subjected to delayed neuronal death is not altered. These observations exclude the possibility that loss of GABAergic innervation is responsible for neuroexcitation leading to neuronal death.